A serious problem during resuscitation to treat sudden cardiac arrest is that, even though defibrillation restores organized cardiac electrical activity, cardiac function is so poor that little or no blood is pumped, a condition called pulseless electrical activity (PEA). One is burst stimulation to restore a pulse pressure during PEA. The other is DC stimulation to improve function during chronic heart failure, which may also be beneficial during PEA. The other is DC stimulation to improve function during chronic heart failure, which may also be beneficial during PEA. In addition to their beneficial effects, these electrical stimuli may also have detrimental effects, the most serious of which is reinitiation of an arrhythmia. The goal of this project is to determine the mechanism of the beneficial and detrimental effects of burst and DC stimulation Electrical and optimal mapping will be used in animals to accomplish three specific aims. Specific Aim 1: To determine the effect of burst and DC stimulation on cardiac nerve activity. The hypothesis will be tested that the primary mechanism by which burst stimulation improves cardiac function is by increasing sympathetic nerve discharge. Specific Aim 2: To determine the effect of burst and DC stimulation on membrane polarization (Vm), action potential (APD), intracellular calcium (Cai/2+), and myocyte motion. The hypothesis will be tested that the primary mechanism by which DC stimulation improves cardiac function is by depolarizing Vm during the AP plateau, thus prolonging APD and increasing Cai2+. Specific Aim 3: To determine the mechanisms of the detrimental effects of burst and DC stimulation. The hypotheses will be tested that the mechanism for tachyarrhythmia induction by burst and DC stimulation are electroporation and creation of a Vm critical point.